Evidence map›Paper›PMID 40304365›Full record

ArticleChinese medical journal2026

Gut microbiota Lactobacillus johnsonii alleviates hyperuricemia by modulating intestinal urate and gut microbiota-derived butyrate.

Rongshuang Han, Zan Wang, Yukun Li, Leyong Ke, Xiang Li, Changgui Li, Zibin Tian, Xin Liu

Abstract read
In one paragraph

Article in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Strain-resolved biology ofFrontiers in veterinary science · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Rongshuang HanDepartment of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, China.
Zan WangDepartment of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, China.
Yukun LiDepartment of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, China.
Leyong KeDepartment of Gastroenterology, Zigong Fourth People's Hospital, Zigong, Sichuan 643000, China.
Xiang LiDepartment of Gastroenterology, Zigong Fourth People's Hospital, Zigong, Sichuan 643000, China.
Changgui LiInstitute of Metabolic Diseases, Qingdao University, Qingdao, Shandong 266003, China.
Zibin TianDepartment of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, China.
Xin LiuDepartment of Gastroenterology, Zigong Fourth People's Hospital, Zigong, Sichuan 643000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGut microbiota are important for uric acid (UA) metabolism in hyperuricemia (HUA); however, the underlying mechanisms of how the gut microbiota regulate intestinal UA metabolism remain unclear. This study aimed to explore the function of the intestine in HUA and to further reveal the possible mechanism.

methodsWe conducted gut microbiota depletion to validate the role of gut microbiota in UA metabolism. A mouse model of HUA was established, and the gut microbiota and microbiome-derived metabolites were analyzed via 16S RNA gene sequencing and metabolomics analysis. The mechanism of the gut microbiota in HUA was elucidated by in vivo and in vitro experiments.

resultsAntibiotic treatment elevated serum UA, disturbed purine metabolism, and decreased the relative abundance of Lactobacillus. HUA mice had a lower relative abundance of Lactobacillus johnsonii (L. johnsonii ) and decreased gut butyrate concentration. Supplementation of L. johnsonii significantly reduces serum UA in hyperuricemia mice by preventing UA synthesis and promoting the excretion of gut purine metabolites. In addition, L. johnsonii enhanced intestinal UA excretion by heightening the urate transporter ABCG2 (adenosine triphosphate-binding cassette transporter, subfamily G, member 2) expression, and increasing the levels of butyrate, which upregulated ABCG2 expression via the Wnt5a/b/β-catenin signaling pathway.

conclusionOur results suggest that gut microbiota and microbiota-derived metabolites directly regulate gut UA metabolism, highlighting potential applications in the treatment of diet-induced HUA by targeting gut microbiota and its metabolites.

Indexed as

ButyratesGastrointestinal MicrobiomeHyperuricemiaLactobacillus johnsoniiUric AcidAnimalsATP Binding Cassette Transporter, Subfamily G, Member 2MaleMiceMice, Inbred C57BLATP Binding Cassette Transporter, Subfamily G, Member 2ButyratesUric AcidButyric acidGut microbiotaHyperuricemiaIntestines

Identifiers

PMID40304365
PMCPMC12767932

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.